Neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio predict in-hospital mortality in symptomatic but unruptured abdominal aortic aneurysm patients.

BACKGROUND: Symptomatic but unruptured abdominal aortic aneurysm (AAA) is a potentially fatal disease since its etiopathogenesis, involving acute changes in the aortic wall, including inflammation, increasing the probability of impending rupture. The objective of the present study was to assess the prognostic value of the neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) in patients undergoing urgent symptomatic AAA repair. METHODS: This was a retrospective study including 29 patients with symptomatic AAA repaired between 2011 and 2020. Both NLR and PLR were calculated on hospital admission prior to the intervention. The primary end point was in-hospital mortality, and the secondary end point included length of hospital stay and postoperative complications. RESULTS: In-hospital mortality rate was 10.3%. The discriminatory performance to predict the primary end point was very good both for PLR (area under the ROC curve [AUC]: 0.92 (95% confidence interval [CI]: 0.82-1.00; P=0.02) and NLR (AUC: 0.88 [95% CI: 0.75-1.00]; P=0.04). The best cutoff point to predict in-hospital mortality was 185 for PLR (100% sensitivity and 85% specificity) and 6.4 for NLR (100% sensitivity and 77% specificity). The most frequent postoperative complication was acute kidney failure (37.9%). Both elevated PLR as NLR were significantly associated with acute kidney failure and multiorgan failure in the immediate postoperative period (P<0.01). None of the two ratios was associated with length of hospital stay (P=NS). CONCLUSIONS: Both PLR and NLR are low-cost inflammatory markers widely available in every emergency department, with excellent performance to predict in-hospital mortality in patients undergoing symptomatic AAA repair. Patients with a PLR≥185 and/or an NLR≥6.4 could benefit from a "surveyed waiting conduct" improving the preoperative clinical condition prior to the intervention, or even considering endovascular repair.

Ozone-induced gene expression occurs via ethylene-dependent and -independent signalling.

Recent studies suggest that ethylene is involved in signalling ozone-induced gene expression. We show here that application of ozone increased glucuronidase (GUS) expression of chimeric reporter genes regulated by the promoters of the tobacco class I beta-1,3-glucanases (GLB and Gln2) and the grapevine resveratrol synthase (Vst1) genes in transgenic tobacco leaves. 5'-deletion analysis of the class I beta-1,3-glucanase promoter revealed that ozone-induced gene regulation is mainly mediated by the distal enhancer region containing the positively acting ethylene-responsive element (ERE). In addition, application of 1-methylcyclopropene (1-MCP), an inhibitor of ethylene action, blocked ozone-induced class I beta-1,3-glucanase promoter activity. Enhancer activity and ethylene-responsiveness depended on the integrity of the GCC boxes, cis-acting elements present in the ERE of the class I beta-1,3-glucanase and the basic-type pathogenesis-related PR-1 protein (PRB-1b) gene promoters. The minimal PRB-1b promoter containing only the ERE with intact GCC boxes, was sufficient to confer 10-fold ozone inducibility to a GUS-reporter gene, while a substitution mutation in the GCC box abolished ozone responsiveness. The ERE region of the class I beta-1,3-glucanase promoter containing two intact GCC boxes confered strong ozone inducibility to a minimal cauliflower mosaic virus (CaMV) 35S RNA promoter, whereas two single-base substitution in the GCC boxes resulted in a complete loss of ozone inducibility. Taken together, these datastrongly suggest that ethylene is signalling ozone-induced expression of class I beta-l,3-glucanase and PRB-1b genes. Promoter analysis of the stilbene synthase Vst1 gene unravelled different regions for ozone and ethylene-responsiveness. Application of 1-MCP blocked ethylene-induced Vst1 induction, but ozone induction was not affected. This shows that ozone-induced gene expression occurs via at least two different signalling mechanisms and suggests an additional ethylene independent signalling pathway for ozone-induced expression of genes involved in phytoalexin biosynthesis.